REL and cancer: The discovery that elevated ΔNp63α leads to activation of NF-κB/c-Rel, a known mediator of inflammatory responses [32], along with the correlation of c-Rel in HNSCC cancer cells harboring high p63 [32,136] levels and the expanded nuclear expression of these proteins in human HNSCC specimen, suggested that coordinated gene regulation by ΔNp63α and c-Rel might explain the heavy immune cell infiltrate typically seen in these poorly responsive SCC [136,137].